(2) Low protein, high GI; (3)High protein, low GI; (4)High protein high GI; (5)Control diet [according to national dietary guidelines]. Their hsCRP levels were compared in the following figure which shows only low GI groups (whether low protein or high protein) have significant reduction in hsCPR levels (P<0.05). The 2 high GI groups (both low protein and high protein) and control group had changes that were statistically non-significant (P>0.05). This might be related to expected reductions of postprandial glucose levels with low-glycemic-index diets, with glucose known to stimulate the expression of inflammatory genes by epigenetic mechanisms. Furthermore, transient increases in glucose induce persistent changes in histone methylation patterns at promoters of inflammatory genes, which is related to glucose-induced mitochondrial generation of oxygen radicals. Long-term increases in basal glucose concentrations are associated with both high fasting insulin concentrations and insulin resistance, which is known to promote inflammatory processes and an increment of hsCRP.
A relatively large study (N=773) done in Europe gives clues to answer the above question. This study is called DiOGenes(Diet, Obesity and Genes study), which is a Randominzed Controlled Trial involving volunteers from 8 European countries. There are 2 parts in this study: 1st part is weight loss phase during which volunteers ate low-calorie diets for 8 weeks and lost weight; 2nd part is weight maintenance phase during which subjects were randomized to 1 of 5 ad libitum diets for 26 weeks. These 5 were (1)Low protein, low glycemic index [GI];
(2) Low protein, high GI; (3)High protein, low GI; (4)High protein high GI; (5)Control diet [according to national dietary guidelines]. Their hsCRP levels were compared in the following figure which shows only low GI groups (whether low protein or high protein) have significant reduction in hsCPR levels (P<0.05). The 2 high GI groups (both low protein and high protein) and control group had changes that were statistically non-significant (P>0.05). This might be related to expected reductions of postprandial glucose levels with low-glycemic-index diets, with glucose known to stimulate the expression of inflammatory genes by epigenetic mechanisms. Furthermore, transient increases in glucose induce persistent changes in histone methylation patterns at promoters of inflammatory genes, which is related to glucose-induced mitochondrial generation of oxygen radicals. Long-term increases in basal glucose concentrations are associated with both high fasting insulin concentrations and insulin resistance, which is known to promote inflammatory processes and an increment of hsCRP.
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